Sunlight plays many important roles for all organisms. Appropriate dosage of sunlight has tremendous biological benefits, such as photosynthesis in plants and vitamin D3 production in human skin [Nemanic M K, Whitney J, Arnaud S, Herbert S, Elias P M. Vitamin D3 production by cultured human keratinocytes and fibroblasts. Biochem Biophys Res Commun 1983; 115:444-50; Holick M F. Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease. Am J Clin Nutr 2004; 80:1678S-88S], especially from exposure to ultraviolet (UV) B radiation. However, overexposure to sunlight will have devastating effects, such as cancer formation [Marrot L, Meunier J R. Skin DNA photodamage and its biological consequences. J Am Acad Dermatol 2008; 58(Suppl):S139-48.], on human beings. Sunlight can cause DNA damage and gene mutation that leads to cancer formation, most typically skin cancer. There are many types of DNA lesions, including the cis-syn, trans-syn, (6-4), and Dewar pyrimidine-pyrimidine photolesions [Taylor J-S. Unraveling the molecular pathway from sunlight to skin cancer. Acc Chem Res 1994; 27:76-82]. Among these possible pyrimidine nucleotide lesions, cis-syn and 6-4 photolesions are commonly observed [Taylor J-S, Cohrs M P. DNA, light and Dewar pyrimidinones: the structure and biological significance of TpT3. J Am Chem Soc 1987; 109:2834-5; Douki T, Court M, Cadet J. Electrospray-mass spectrometry characterization and measurement of far-UV-induced thymine photoproducts. J Photochem Photobiol B 2000; 54:145-54; Rochette P J, Therrien J P, Drouin R, Perdiz D, Bastien N, Drobetsky E A, et al. UVA-induced cyclobutane pyrimidine dimers form predominantly at thymine-thymine dipyrimidines and correlate with the mutation spectrum in rodent cells. Nucleic Acids Res 2003; 31:2786-94]. Furthermore, the pyrimidine (6-4) pyrimidone photolesion is very mutagenic [Glas A F, Schneider S, Maul M J, Hennecke U, Carell T. Crystal structure of the T(6-4)C lesion in complex with a (6-4) DNA photolyase and repair of UV-induced (6-4) and Dewar photolesions. Chemistry 2009; 15:10387-96; Thomas M, Guillaume D, Fourrey J L, Clivio P. Further insight in the photochemistry of DNA: structure of a 2-imidazolone (5-4) pyrimidone adduct derived from the mutagenic pyrimidine (6-4) pyrimidone photolesion by UV irradiation. J Am Chem Soc 2002; 124:2400-1; Young A R, Chadwick C A, Harrison G I, Hawk J L, Nikaido O, Potten C S. The in situ repair kinetics of epidermal thymine dimers and 6-4 photoproducts in human skin types I and II. J Invest Dermatol 1996; 106:1307-13], thereby leading to cancer formation.
Skin cancer is currently the most common type of human cancer in the United States [Jung S K, Lee K W, Byun S, Kang N J, Lim S H, Heo Y S, et al. Myricetin suppresses UVB-induced skin cancer by targeting Fyn. Cancer Res 2008; 68:6021-9]. Because DNA damage usually leads to cancer, tremendous attention has been given to damaged DNA repair research [Young A R, Chadwick C A, Harrison G I, Hawk J L, Nikaido O, Potten C S. The in situ repair kinetics of epidermal thymine dimers and 6-4 photoproducts in human skin types I and II. J Invest Dermatol 1996; 106:1307-13; Shimura T, Martin M M, Torres M J, Gu C, Pluth J M, DeBernardi M A, et al. DNA-PK is involved in repairing a transient surge of DNA breaks induced by deceleration of DNA replication. J Mol Biol 2007; 367:665-80; Ueta E, Sasabe E, Yang Z, Osaki T, Yamamoto T. Enhancement of apoptotic damage of squamous cell carcinoma cells by inhibition of the mitochondrial DNA repairing system. Cancer Sci 2008; 99:2230-7; Brissett N C, Doherty A J. Repairing DNA double-strand breaks by the prokaryotic non-homologous end-joining pathway. Biochem Soc Trans 2009; 37:539-45]. In addition to endogenous DNA repair systems, DNA damage prevention, such as protection from UV radiation, can greatly minimize cancer formation. In general, skin application of sunscreen products, which block the UV from sunlight that causes the DNA damage, can effectively minimize DNA photolesion formation and prevent human skin cancer development. Many medical agencies have also recommended the use of sunscreens to temporarily protect the skin from sunlight exposure [Autier P, Boniol M, Dore J F. Sunscreen use and increased duration of intentional sun exposure: still a burning issue. Int J Cancer 2007; 121:1-5; Sayre R M, Dowdy J C, Lott D L, Marlowe E. Commentary on ‘UVB-SPF’: the SPF labels of sunscreen products convey more than just UVB protection. Photodermatol Photoimmunol Photomed 2008; 24:218-20].
To evaluate the effectiveness of sunscreen products, human subjects are normally used. Measurements of sunscreen effectiveness are performed by administering different sunscreen dosages to volunteers and then exposing them to sunlight [Young A R, Chadwick C A, Harrison G I, Hawk J L, Nikaido O, Potten C S. The in situ repair kinetics of epidermal thymine dimers and 6-4 photoproducts in human skin types I and II. J Invest Dermatol 1996; 106:1307-13; Jung S K, Lee K W, Byun S, Kang N J, Lim S H, Heo Y S, et al. Myricetin suppresses UVB-induced induced skin cancer by targeting Fyn. Cancer Res 2008; 68:6021-9; Young A R, Potten C S, Chadwick C A, Murphy G M, Hawk J L, Cohen A J. Photoprotection and 5-MOP photochemoprotection from UVR-induced DNA damage in humans: the role of skin type. J Invest Dermatol 1991; 97:942-8; Bissonnette R, Allas S, Moyal D, Provost N. Comparison of UVA protection afforded by high sun protection factor sunscreens. J Am Acad Dermatol 2000; 43:1036-8; Young A R, Sheehan J M, Chadwick C A, Potten C S. Protection by ultraviolet A and B sunscreens against in situ dipyrimidine photolesions in human epidermis is comparable to protection against sunburn. J Invest Dermatol 2000; 115:37-41; Wagner J K, Parra E J, L Norton H, Jovel C, Shriver M D. Skin responses to ultraviolet radiation: effects of constitutive pigmentation, sex, and ancestry. Pigment Cell Res 2002; 15: 385-90; Kelly D A, Seed P T, Young A R, Walker S L. A commercial sunscreen's protection against ultraviolet radiation-induced immunosuppression is more than 50% lower than protection against sunburn in humans. J Invest Dermatol 2003; 120: 65-71; Dupuy A, Dunant A, Grob J J. Randomized controlled trial testing the impact of high-protection sunscreens on sunexposure behavior. Arch Dermatol 2005; 141:950-6; Moyal D D, Fourtanier A M. Broad-spectrum sunscreens provide better protection from solar ultraviolet-simulated radiation and natural sunlight-induced immunosuppression in human beings. J Am Acad Dermatol 2008; 58(Suppl):S149-54]. This strategy is costly and allows for difficulty in generalizability because of age, sex, and race differences among the subjects. It is also difficult to cross-validate the quality and effectiveness of different sunscreen products. Moreover, with the traditional methods, it is difficult to develop highthroughput screening for highly efficient and less toxic sunscreens, which are needed to reduce cancer formation, especially skin cancer formation. Unfortunately, there is no simple, efficient, and quantitative methodology to address these cross-validation, high-throughput, and effectiveness questions using sunscreen products with human or animal subjects [Diffey B L, Tanner P R, Matts P J, Nash J F. In vitro assessment of the broad-spectrum ultraviolet protection of sunscreen products. J Am Acad Dermatol 2000; 43:1024-35; Wang S Q, Stanfield J W, Osterwalder U. In vitro assessments of UVA protection by popular sunscreens available in the United States. J Am Acad Dermatol 2008; 59:934-42].
Therefore, there is a need existing for the development of simple, convenient, efficient, effective, inexpensive, and/or quantitative systems and methods to evaluate the sunscreen efficacy.